Autism Spectrum Disorders (ASD) is a multifactorial neurodevelopmental pathology, resulting from a combination of genetic and environmental factors. However, the contribution of each of these two components to the onset and/or the evolution of ASD remains undetermined. Hence the aim of our research project is to evaluate the impact of an in utero exposure to a cocktail of fungicide residues at a European regulatory dose on the brain development of a well-established ASD model, the CNTNAP2 gene-deficient mouse. In order to determine whether the chronic exposure to fungicide might increase the severity of ASD behavioral symptoms (stereotypies and social interaction deficits) and the extent of cortical malformations, we performed in utero electroporation of MAGIC Markers in wild-type (WT), heterozygous (het) and knock-out (KO) CNTNAP2 littermates which have been exposed chronically during gestation and lactation to a cocktail of fungicide residues, compared to non-treated controls. Triggering this multicolor fate mapping strategy at the beginning of cortical neurogenesis enables the tracking of cortical progenitors and their neuronal and glial descents from early to late stages of cerebral cortex development. Therefore, discrete and heterogeneous cortical malformations can be reported in male and female individuals displaying various ASD-like behaviors assessed by standardized behavioral tests performed at distinct developmental stages (P3-P7-P21-P60) in several groups according to their respective genotype and treatment. This work will give us a better understanding of the possible synergy between environmental factors and genetic predisposition in the establishment and evolution of ASD, while pointing to new cellular and molecular therapeutic targets.